ライフサイエンスコーパス: Th2

1 We found that low Th1/Th2 activity ratios were associated with a significantly

2 Pursuing the Th2 adaptive immune response further we demonstrate that

3 revent allergen sensitization and subsequent Th2 allergic inflammation.

4 However, a Th2 allergic inflammatory response is suggested by the p

5 Treatment of mucosa with Th2 and fibrotic cytokines recapitulated the majority of

6 ith a cytokine cocktail to closely mimic the Th2 and inflammatory milieu of eosinophilic esophagitis

7 by myeloid cells, which then cross-regulated Th2 and regulatory T cells.

8 fic deletion of Kdm6a showed upregulation of Th2 and Th1 activation pathways and downregulation of ne

9 se a subpopulation expressing high levels of Th2 and Th17 cytokines, chemokine receptors CCR4 and CCR

10 D4(+) T cells display a prominent feature of Th2 and Th17 differentiation and exert high efficacy and

11 1 and Th17 responses and the upregulation of Th2 and Th9 responses.

12 number and activation of LC, while enhancing Th2 and Tr1 responses upon epicutaneous protein sensitiz

13 e, prevented Th1 infiltration, and increased Th2 and Treg levels.

14 Conversely, the cooperative action between Th2 and Tregs subsets creates an anti-inflammatory and p

15 es C), they enhanced commitment to IL4/5/13 (Th2) and away from IFNg (Th1).

16 showed significant cytokine responses (Th1, Th2, and granulocyte-macrophage colony-stimulating facto

17 , is associated with elevated levels of TH1, TH2, and proinflammatory cytokines, indicating an associ

18 tionally analogous to T helper type 1 (Th1), Th2, and Th17 cells are well characterized, an ILC subse

19 es in cytokine production were found in Th1, Th2, and Th17 immunity in response to both unspecific an

20 estine associated with helper T cells' (Th1, Th2, and Th17) specific pathways.

21 TCC secreted Th1, Th2, and Th22 cytokines and effector molecules and expre

22 with upstream drivers including hallmark Th1/Th2- and inflammation-associated genes.

23 Th2-antagonistic type1 IFN signalling may play a key rol

24 s, cytokine production, and proliferation of Th2 as well as Tregs.

25 cted, INF individuals had elevated levels of TH2-associated and regulatory cytokines that normalized

26 IL-33 primarily induces the production of Th2-associated cytokines but acts as an "alarmin" via st

27 Tg+ mice had significantly reduced levels of Th2-associated gene signatures (Slc26a4, Clca1, Retnla,

28 terestingly, at later time points, levels of Th2-associated interleukin-4 (IL-4) and IL-10 were also

29 y features, including elevated expression of Th2-associated markers accompanied by MCM, elevated MUC5

30 g merging of FOXP3/IL2-with inflammation-and Th2-associated modules.

31 ected by deliberate changes in the early Th1/Th2 balance.

32 Allergic asthma (AA) is characterized as a Th2-biased airway inflammation that can develop lung inf

33 IgE is the central antibody isotype in TH2-biased immunity and allergic diseases.

34 In atopic asthma, chronic Th2-biased inflammation is associated with an increased

35 In contrast, all aPV vaccines showed a Th2-biased response.

36 s, we showed that Trim32 null mice developed Th2-biased skin inflammation in response to imiquimod an

37 here, IL-4M induced a sustained decrease of Th2-biased Tregs (ST2(+) FOXP3(+) GATA3(intermediate) ).

38 the number of potentially disease-triggering Th2-biased Tregs was further significantly decreased by

39 al skin showed significant dysregulations of Th2 (CCL17 and IL4R) and Th22/Th17 (IL36G, CCL20, and S1

40 he ratio of CXCR5IFN-gammaCD8 T cells to Th1/Th2 CD4 T cells) may identify recipients at risk for dev

41 ection, ASC depletion impaired lung ILC2 and Th2 cell accumulation and function, which are in part de

42 3 expression in an antigen-primed developing Th2 cell are not well understood.

43 uced interleukin-12 (IL-12), which prevented Th2 cell development by promoting T-bet upregulation in

44 ter of GATA3 expression that is critical for Th2 cell development in the lung to inhaled but not syst

45 ctivation to up-regulate Blimp-1 and promote Th2 cell development.

46 at TRIM32 deficiency contributes to enhanced Th2 cell differentiation in vitro.

47 Th1 and Th2 cell modes of motility could be switched simply by m

48 te motility gene programs that shape Th1 and Th2 cell navigation of the inflamed dermis.

49 During exacerbation, peripheral blood Th2 cell numbers correlated with ACQ6 and AQLQ scores, w

50 eover, a MRTF signature is correlated with a Th2 cell signature in human PDA tumors.

51 CXCR5IFN-gammaCD8 T cell to combined CD4 Th1/Th2 cell subsets (IFN-gammaCD4 and IL-4CD4 cells; P = 0.

52 Recent identification of memory Th2 cell subsets that are characterized by high receptor

53 t, upregulation of T helper type 1 (Th1) and Th2 cell-associated pathways, including interferon respo

54 Interestingly, IL-3R(+) cells exhibit a Th2 cell-like phenotype and show high GATA-3 expression.

55 critically contributes to the development of Th2 cell-mediated disorders, most likely by influencing

56 Supported by a mixed Th1/Th2 cell-mediated immunity, P27A induced a marked specif

57 Specifically, IL18 induced a Th2 cell-mediated response in the absence of IL12.

58 ote inflammation and simultaneously induce a Th2 cell-mediated response via IL18.

59 ced activation of T cells and no increase in Th2 cell-mediated responses compared with control mice.

60 amine receptor (DRD4) to promote T helper 2 (Th2) cell differentiation.

61 Although T-helper type 2 (Th2) cell pathology is implicated in severe disease, the

62 hether cDC1s also control CD4(+) T helper 2 (Th2) cell responses, since suppressive and activating ro

63 whole blood flow cytometry: CD4(+) T cells, Th2 cells (CD4(+) CRTh2(+) T cells and % of CD4(+) T cel

64 nt receptor-homologous molecule expressed on Th2 cells (CRTH2), a receptor for the bioactive lipid pr

65 hemoattractant receptor homolog expressed on Th2 cells (CRTH2)-expressing CD4(+) and CD8(+) T cells d

66 creased numbers of intestinal Th17 cells and Th2 cells and decreased numbers of RORgammat(+) Treg cel

67 ls but increases in interleukin 5-expressing Th2 cells and eosinophils in perigonadal and inguinal AT

68 te that Th2 Trm cells and circulating memory Th2 cells are functionally and transcriptionally distinc

69 from mice with pancreatitis had increases in Th2 cells but not in Th1 cells.

70 y Th2 (Th2 Trm) cells and circulating memory Th2 cells collaborate in vivo remain unclear.

71 vealed that while Notch-deficient lymph node Th2 cells established competence for lung migration, the

72 This is because Malat1(-/-) Th1 and Th2 cells express lower levels of the immunosuppressive

73 ion of the Gata3 promoter detectable only in Th2 cells for EPIT from the 4th week and a significant h

74 PKCzeta that controls the differentiation of Th2 cells important for AD pathogenesis.

75 Raif Geha, they studied the role of Th2 cells in allergic responses and he began work in Kaw

76 These data suggest that Th2 cells in peripheral blood may be a sensitive measure

77 Moreover, Th2 cells in presence of IL-3 show increased expression

78 on of naive CD4(+) T cells to Th17, Th1, and Th2 cells led to significant increase in Lcn2 expression

79 ith EoE convtained a prominent population of Th2 cells not seen in controls.

80 te that Th2 Trm cells and circulating memory Th2 cells perform nonredundant functions.

81 roles in host protection against TB, whereas Th2 cells producing IL-4 and regulatory T cells (Tregs)

82 GPCR) and chemokine-dependent fashion, while Th2 cells scanned a larger tissue area independent of GP

83 ed that Th2 Trm cells and circulating memory Th2 cells share a core Th2 gene signature but also exhib

84 Instead, Notch-deficient in vitro-polarized Th2 cells showed reduced accumulation in the lungs upon

85 Upon HDM rechallenge, circulating memory Th2 cells trafficked into the lung parenchyma and ignite

86 It acts by attracting regulatory T cells and Th2 cells via their receptor CCR type 4 (CCR4).

87 r and allergen challenge, as Notch-deficient Th2 cells were retained in the lung-draining lymph nodes

88 PKCzeta stability tended to be increased in Th2 cells with a Trim32 null background.

89 e in inhibiting the Th1 program in committed Th2 cells, and mechanistically, its role might relate to

90 Differentiation of T-helper (Th1) cells, Th2 cells, and T-regulatory cells was determined by nucl

91 pecific enrichment of CD4+ Treg and effector Th2 cells, confinement of type 2 cytokine production to

92 complex, expressed primarily on mast cells, Th2 cells, group 2 innate lymphoid cells and regulatory

93 urden of SCNAs have high levels of Tregs and Th2 cells, highlighting the importance of evaluating evo

94 cing Th1 cells, interleukin-(IL)-4-producing Th2 cells, IL-17-producing Th17 cells, follicular T help

95 o its receptor ST2 on targets such as CD4(+) Th2 cells, ILC2, and mast cells.

96 ophil-rich pulmonary type 2 immune response (Th2 cells, M2 macrophages, type 2 innate lymphoid cells,

97 itro-polarized Th1 and Th17 cells but low in Th2 cells, suggesting that this lncRNA may regulate infl

98 and IL-3 regulates the effector functions of Th2 cells.

99 eading to increased GATA3 expression in lung Th2 cells.

100 HPGDS+ CRTH2+IL-17RB+FFAR3+CD4+ T8 effector Th2 cells.

101 cells that were unable to suppress extrinsic Th2 cells.

102 type 2 lymphocytes, NKT, and CD4(+) CRTH2(+) Th2 cells.

103 and is downregulated in Malat1(-/-) Th1 and Th2 cells.

104 ukin (IL)-4, IL-5 and IL-13 from T helper 2 (Th2) cells and innate lymphoid cells type 2 (ILCs), and

105 T helper type 2 (Th2) cells are important regulators of mammalian adaptiv

106 Memory CD4+ T helper type 2 (Th2) cells drive allergic asthma, yet the mechanisms whe

107 sease severity would correlate with enhanced Th2 cellular responses.Methods: Nasal aspirates were col

108 lper cell type 2 (Th2) cytokine genes or the Th2 chemokine genes CCL11, CCL17, and CCL22.

109 Notably, plasma levels of the TH2 chemokines CCL17 and CCL22 are also elevated during

110 expression levels of T helper cell-mediated (TH2) chemokines CCL18, CCL17, and CCL22 by ELISA in plas

111 ude increased lung CD4(+) T cells, increased Th2 cytokine expression, and airway goblet cell hyperpla

112 epidermal thickness, lower total serum IgE, Th2 cytokine levels and CD4(+) effector T cell populatio

113 , lung histology, and elevated pulmonary Th1/Th2 cytokine levels.

114 Ligands for FFAR3 induced Th2 cytokine production from human and murine T cells, i

115 lic infiltration, collagen accumulation, and Th2 cytokine production in allergic airways.

116 y inflammation, goblet cell hyperplasia, and Th2 cytokine production were attenuated in WT mice that

117 y inflammation, goblet cell hyperplasia, and Th2 cytokine production, including IL-4, IL-5, and IL-13

118 irway inflammation and significantly reduced Th2 cytokine production, serum IgE levels, and airway hy

119 nized animals showed significantly decreased Th2 cytokine responses, cow's milk-specific IgE remained

120 ells expanded and differentiated into Th1 or Th2 cytokine-producing effectors in a manner similar to

121 entiation and recruitment, and IL-4, a major Th2 cytokine.

122 reciprocal increase of T-helper cell type 2 (Th2) cytokine genes or the Th2 chemokine genes CCL11, CC

123 Our data demonstrate multiplicity of Th2-cytokine control of eosinophil tissue recruitment du

124 ytokines (IL-2 and IFN-gamma) as compared to Th2 cytokines (IL-4 and IL-5) in splenocyte culture supe

125 entrations of asthma-associated prototypical Th2 cytokines also stimulate the carotid bodies.

126 ost prominent effect was on the reduction of Th2 cytokines and IL-10 in PBMC cultures.

127 Local tissue eosinophilia and Th2 cytokines are characteristic features of seasonal al

128 sed gastric mucosal levels of Th1, Th17, and Th2 cytokines compared with Nod1 wild-type (WT) mice.

129 ransplantation diminishes pathology, reduces Th2 cytokines in muscle and biases macrophages away from

130 Nasal symptoms, Th1/Th2 cytokines in nasal secretion and serum were evaluate

131 midine treatment induced a shift from Th1 to Th2 cytokines in the serum and an increase in the freque

132 The Th2 cytokines interleukin 4 (IL-4) and IL-13 and the het

133 tion of tolerogenic cytokines, inhibition of Th2 cytokines production and a modulation of oxidative s

134 epletion reduces lung ILC2 proliferation and Th2 cytokines suggesting ILC2 function is influenced by

135 2-biased disease with elevated expression of Th2 cytokines that responds to Th2 signaling blockade.

136 provides evidence for the ability of Th1 and Th2 cytokines to determine PTB status in AFB microscopy

137 nd Th17 cytokines and reducing expression of Th2 cytokines upon coculture with CD4(+) T cells.

138 sensitive to asthma-associated prototypical Th2 cytokines which elicit sensory nerve excitation.

139 cell protease 1 (Mcpt-1) and Mcpt-4, Th1 and Th2 cytokines, and patterns of ileal mastocytosis and in

140 argeting Hsp70 to alleviate allergen-induced Th2 cytokines, goblet cell hyperplasia, and airway infla

141 ion correlated with suppression of two major Th2 cytokines, IL-10 and IL-13.

142 hat outcompeted immunosuppressive effects of TH2 cytokines, whereas HBV coinfection did not alter sch

143 plasia, elevated serum Igs, and induction of Th2 cytokines.

144 ently discovered immune population secreting Th2 cytokines.

145 d genomic stability as well as production of Th2 cytokines.

146 h) 1 and Th17 cytokines and higher levels of Th2 cytokines.

147 ith higher levels of therapy-induced IgE and TH2 cytokines.

148 wounding by producing type 2 T helper cell (Th2) cytokines in mice.

149 s (ILC2s) are a potent source of T-helper 2 (Th2) cytokines that promote AHR and lung inflammation.

150 rate that tyrosine-hydroxylase-2-expressing (th2+) DA neurons in the zebrafish hypothalamus fire phas

151 TH2-derived IL-31 is involved in IBH pathology and accor

152 ng HDM sensitization in C57Bl/6 mice blocked Th2 development.

153 ction of main cytokines that promote Th1 and Th2 differentiation, and the induction of allergen-speci

154 al and genetic data, we provide an atlas for Th2 differentiation, validating known regulators and ide

155 tiation and Treg formation without impacting Th2 differentiation.

156 n leading to diminished Th1/17 but unchanged Th2 differentiation.

157 for the development of type 2 T-helper cell (Th2)-driven inflammatory disorders and has also been imp

158 ring Tnfaip3-deficient cDC1s did not develop Th2-driven eosinophilic airway inflammation upon HDM exp

159 o investigate the role of activated cDC1s in Th2-driven immune responses, pulmonary cDC1s were activa

160 tegration of mite-induced Th cell-associated Th2-, FOXP3/IL2-, inflammation- and finally type1 IFN-si

161 ated network module and its merging into the Th2/FOXP3/IL2/inflammation module.

162 educing inhibitory histone trimethylation at Th2 gene loci.

163 nd circulating memory Th2 cells share a core Th2 gene signature but also exhibit distinct transcripti

164 art of the core regulatory network governing Th2 helper cell fates.

165 the differentiation of T cells into Th1 and Th2 helper cells that mediate cell-based and humoral imm

166 10-fold lower fungal burden and with greater Th2 (IL-13) immune response.

167 L-4/IL-13 signaling is a key driver of type2/Th2 immune diseases (atopic/allergic diseases).

168 This study aims to determine Th2 immune parameters in patients presenting to the emer

169 te cytokine production to promote an altered Th2 immune response following RSV infection that leads t

170 de parasite T.muris, which requires adaptive Th2 immune response for elimination.

171 A Th2 immune response is central to allergic airway inflam

172 other adjuvants utilized in AIT redirect the Th2 immune response towards Th1 immunity.

173 g a potential mixed and antigen-specific Th1/Th2 immune response, which is different from the Th2 imm

174 Th2 immune responses are often manifested as increased m

175 33 are consistently associated with adaptive Th2 immune responses in asthma.

176 IL-33 is a known inducer of Th2 immune responses, but its roles in mucus obstruction

177 induced by ovalbumin (OVA), we investigated Th2 immune responses, M2 macrophage activation and skin

178 characterized by defective skin barrier and Th2 immune responses.

179 survival effects in ccRCC, primarily through Th2 immune- and NRF2-dependent macrophage networks.

180 istent with an unrestrained T helper type 2 (Th2) immune response.

181 ated with the suppression of casein-specific Th2 immunity and induced Th1 and Th17 cytokines as well

182 rt that prior to influencing activation, Th1/Th2 immunity first controls the size of the permissive h

183 immune response, which is different from the Th2 immunity induced by the natural saponin MS I.

184 Th2 immunity involves a shift of the CD4(+) T-cell popul

185 The impact of T helper (Th) 1 versus Th2 immunity on intracellular infections is attributed t

186 demonstrate deficiencies in mediators of Th1-Th2 immunity, which have paradoxical or no impact.

187 own for its ability to induce a balanced Th1/Th2 immunity.

188 A skewing of immune responses toward Th2 in transplant patients appears to confer protection

189 hR, we detected an enhanced T helper type-2 (Th2) [increased interleukin 5 (IL-5) and interleukin 13

190 to DEP mediated increase in allergen-induced Th2 inflammation and AHR in a mouse model of severe ster

191 n homologue YKL-40, plays important roles in Th2 inflammation and allergen sensitization.

192 xposure, the dopamine-DRD4 pathway augmented Th2 inflammation in the lungs of young mice.

193 development of AD induced by OVA, affecting Th2 inflammation, M2 macrophage activation and skin barr

194 Our data support no link between robust Th2-inflammation and development of airway remodelling i

195 interstitial airspaces and the activation of Th2 inflammatory and profibrotic pathways in experimenta

196 data indicate that although IL-33 modulates Th2 inflammatory responses and MUC5AC protein production

197 t extent the vagus nerve is of importance in Th2 inflammatory responses like food allergy is still un

198 c T-cell compartments with downregulation of Th2 key regulators and upregulation of Treg transcriptio

199 nalogues 5 and 6 that probably only induce a Th2-like immunity.

200 -4/13B are required for the maintenance of a Th2-like phenotype in the gills and the suppression of t

201 Th2-like Treg cells showed increased intra-chromosomal i

202 ptional program leading to the generation of Th2-like Treg cells that were unable to suppress extrins

203 reased intra-chromosomal interactions in the Th2 locus, leading to type 2 cytokine production.

204 es exhibited suppressed expression levels of Th2 markers, diminished MCM, suppressed MUC5B expression

205 egative correlations were identified between Th2 measures and epidermal barrier gene-subsets and indi

206 a primary Ascaris infection, such that CD4+ Th2-mediated eosinophil-dependent helminth larval killin

207 exposed to house dust mite (HDM) to provoke Th2-mediated immune responses.

208 AD can exacerbate extrinsic AD by augmenting Th2-mediated inflammation and mast cell activation.

209 ccumulation in the skin lesions, more severe Th2-mediated inflammation, including higher serum IgG1 a

210 After 22 weeks, a typical type 2/Th2-mediated inflammatory profile was obtained, as demon

211 Additionally, the Th2 modulatory response was evaluated in IL-4 reporter m

212 CD4 T-cell responses and low or undetectable Th2 or CD8 T-cell responses.

213 rvations expand our understanding of the Th1-Th2 paradigm during infection.

214 transcription factors and framing of the Th1/Th2 paradigm ignited the CD4(+) T cell field.

215 ell percentages, and stable naive CD8(+) and Th2 percentages across groups.

216 pletely rescued in IFN-gamma-deficient or in TH2 phase coinfected mice demonstrating the key role of

217 T cells are unable to differentiate into the Th2 phenotype, and acquire a Th17-like phenotype in resp

218 ay analysis predicted the miRNAs to regulate Th2 polarization and dendritic cell maturation.

219 an ideal tool for noninvasive monitoring of Th2 polarization and straightforward identification of i

220 Gal-3 has been shown to regulate Th1/Th2 polarization of CD4(+) T cells; however, the extent

221 was not required for T cell proliferation or Th2 polarization.

222 In a reporter mouse, the mimetic inhibited Th2 polarization.

223 In contrast, in Th2-polarized settings such as house dust mite-induced a

224 Two of the vaccines induced a Th2-predominant response and the other a Th1-predominant

225 ratory allergen exposure and counteracts the Th2 priming effect of CysLT1R signaling at sensitization

226 ay molecular phenotype that has elevated Th1/Th2 ratios.

227 anulocytic expression of integrin CD11b, and Th2-related CRTH2 downregulation in eosinophils and baso

228 This was accompanied by up-regulation of the Th2-relevant transcription factor GATA3 and reduction in

229 rapies that target key molecules driving the Th2 response are already used in the clinic, and a wave

230 uggable Notch signaling pathway licenses the Th2 response in allergic airway inflammation via promoti

231 ht be involved in the early development of a Th2 response in the airways and asthma.

232 1 circuit as an initiator of an inflammatory Th2 response in the lung to allergens.

233 t cancer patients, whereas an unbalanced Th1/Th2 response was correlated with poorer survival of colo

234 iters of antibodies and elicited a mixed Th1/Th2 response.

235 ophilin-5 regulates IL-33 production and the Th2 response.

236 Prominent gene pathways involved the Th2-response, de novo cholesterol synthesis, fructose an

237 soluble egg antigens (SEAs) to induce robust Th2 responses and airway inflammation in the lungs.

238 drug known to modulate T-helper type 1 (Th1)/Th2 responses and has the potential to regulate immunity

239 Notably, BcfA strongly attenuated the Th2 responses elicited by FHA and Prn, resulting in Th1/

240 ection regimes that promote distinct Th1 and Th2 responses in C57BL/6 mice.

241 ly likely role for FFAR3 in amplifying local Th2 responses in EoE, and a resource to further dissect

242 associated with suppression of lung-specific Th2 responses long after initial treatment.

243 re balanced IgG1:IgG2a/IgG2b-derived Th1 and Th2 responses than LcrV-immunized mice.

244 Allergic asthma is mediated by Th2 responses to inhaled allergens.

245 on adjuvant that redirects allergen-specific Th2 responses toward Th1 and Th17 immunity, and protects

246 able homeostatic control of allergen-induced Th2 responses via cross-regulation.

247 or IFNgamma in Tnfaip3(Lg-KO) mice restored Th2 responses, whereas administration of recombinant IFN

248 Aluminium hydroxide initially boosts Th2 responses, while the other adjuvants utilized in AIT

249 s of HDM, DEP increases IL33 lung levels and Th2 responses.

250 ators of osteoclastogenesis and mediators of Th2 responses.

251 okine IL-33 is a well-established inducer of Th2 responses.

252 eg) cell differentiation and inhibit Th1 and Th2 responses.

253 duce the nonprotective T helper cell type 2 (Th2) responses characteristic of wild-type infection, in

254 letion enhanced IL-33 release and pathogenic Th2 responsiveness through the mTOR pathway and altered

255 expression of Th2 cytokines that responds to Th2 signaling blockade.

256 rotein that contributes to the regulation of Th2 signaling.

257 The preterm infants were also more Th2 skewed than the full-term infants.

258 ing in Th1/17-skewed responses in inherently Th2-skewed BALB/c mice.

259 immune signaling, complement dysregulation, Th2 skewing, and increased secretion of MCP-1.

260 elease of substance P to induce migration of Th2-skewing CD301b(+) DC to draining lymph nodes.

261 Th2 switch, while TRPV1 agonists mediated a Th2 switch at 37 degrees C.

262 ritic cells (DCs) at fever temperatures, the Th2 switch was abrogated via increased production of IL1

263 The febrile Th2 switch was IL4 independent, but a gamma-secretase in

264 e TRPV1/TRPV4 antagonism blocked the febrile Th2 switch, while TRPV1 agonists mediated a Th2 switch a

265 function of basophils resulted in a blunted Th2 T cell response to a protein allergen.

266 encies of monofunctional and dual functional Th2/Tc2 and Th9/Tc9 cells with parasite antigen stimulat

267 nal Th1/T cytotoxic type 1 (Tc1), Th17/Tc17, Th2/Tc2, and Th9/Tc9 cells in S. stercoralis infection i

268 Th2-, Th1-, Th9- and Tr1-type cytokines decreased over t

269 ells of VL patients, associated with reduced Th2, Th17, and FOXP3+CD4+ T regulatory cell frequencies

270 mposition comprised of higher frequencies of Th2, Th17, and Tc17 cells compared to the peripheral blo

271 e of cytokine responses, by stimulating Th1, Th2, Th17, and Tfh cytokines.

272 (+) , IgE(+) and IgA(+) memory B cells, Th1, Th2, Th17, and Treg-memory cells from venous blood.

273 and mouse CD4 T cells were activated in Th1, Th2, Th17, or regulatory T cell (Treg) environments with

274 The expression levels of Th1, Th2, Th17, or T regulatory-associated cytokines and RANK

275 rentiation program, while the development of Th2, Th17, Tfh, and Treg cells is dependent on transcrip

276 fector program [e.g., T helper type 1 (Th1), Th2, Th17].

277 at show a similar helper T-cell profile with Th2/Th17 predominance.

278 c cells and IL33 pulsed BMDC promote a mixed Th2/Th17 response that was dependent on ST2 expression b

279 regulatory T cell expression and suppressed Th2/Th17 response.

280 ctional FOXP3(+) Treg cells and promotes Th1/Th2/Th17 responses.

281 ype, SLT patients have an increased ratio of Th2:Th17 cells.

282 assium (+2 mM), or magnesium (+1 mM) reduces Th2:Th17 ratio and augments Th17 polarisation.

283 he mechanisms whereby tissue-resident memory Th2 (Th2 Trm) cells and circulating memory Th2 cells col

284 ch signaling activates expression of the key Th2 transcription factor Gata3, it remains controversial

285 hIP revealed a specific de-repression of the Th2 transcriptional program leading to the generation of

286 Children with any atopic disease had higher Th2, Treg, Treg-memory, and CD27(+) IgA(+) memory B-cell

287 Our findings demonstrate that Th2 Trm cells and circulating memory Th2 cells are funct

288 c asthma and parabiosis, we demonstrate that Th2 Trm cells and circulating memory Th2 cells perform n

289 Transcriptional analysis revealed that Th2 Trm cells and circulating memory Th2 cells share a c

290 Th2 Trm cells express a tissue-adaptation signature, inc

291 In contrast, Th2 Trm cells proliferated near airways and induced mucu

292 chanisms whereby tissue-resident memory Th2 (Th2 Trm) cells and circulating memory Th2 cells collabor

293 where they play a role in the production of Th2-type cytokines.

294 ammatory cytokine production that promotes a Th2-type immune environment.

295 Intestinal helminth infections elicit Th2-type immunity, which influences host immune response

296 Th2-type isotype IgG1 antibody levels were associated wi

297 xpression modules including those related to Th2-, type1 IFN-, inflammation- and FOXP3/IL2-associated

298 onse than RV-A without T-helper cell type 2 (Th2) upregulation.

299 lungs and blood, decreased Th1 response, and Th2 weighted shift.

300 (+) T-cell population from type-0 to type-2 (Th2) with increased abundance of interleukin (IL)-4 and